离体培养动脉内皮细胞结合、内移和降解脂蛋白(α)作用的研究

The study of binding, internalization and degrradation of lipoprotein(α) in aortic endothelial cells in vitro

本文研究离体培养动脉内皮细胞通过LDL受体结合、内移和降解脂蛋白(α)[lipopro-tein(a),Lp(α)]的作用.实验取第3～4代离体培养的动脉内皮细胞分为两组,对照组培养液中不加碘标的脂蛋白(a)[^(125)I—Lp(α)],实验组培养液中加^(125)I—Lp(α)最终浓度分别为0.25、0.5、1、10和50μg/ml.用γ计数器测定内皮细胞对Lp(α)的结合、内移和降解值,并测定内皮细胞的蛋白质量,以μg/mg细胞蛋白表示.结果随培养液中加进^(125)I—Lp(α)的浓度递增而增加,在10μg/ml浓度时最大的结合、内移和降解值分别是0.219、0.390和0.465μg/mg细胞蛋白;最大的结合率、内移率和降解率分别是2.19%、3.90%和4.65%.结果提示Lp(α)通过动脉内皮细胞LDL受体途径的摄取和降解作用是非特异性的.

The role of binding, internalization and degradation of lipoprotein (α)[Lp(α)] in the aortic endothelial cells (AEC) through LDL receptors were studied in vitro. Bottles of AEC were divided into control group and experimental groups after 3 - 4 passages of subcultule. 125I labelled Lp(α) was added to the experimental groups in a concentration of 0. 25, 0. 5, 1. 0, 10. 0, and 50. 0ug/ml of medium, but none was added to the control group. The binding, internalization and degradation of Lp(α) in AEC through LDL receptors were assayed for radioactivity. When the concentration of 125I-Lp(α) was less than 10. 0ug/ml, the value of binding, internalization and degradation was increased steadily up to the maximum of 0. 129ug, 0. 39ug and 0. 465ug/mg cell protein respectively. Results suggested nonspecial uptake and degradation of Lp(α) in the AEC through LDL- receptors -mediated pathway.